No Arabic abstract
Microbial dormancy is an evolutionary trait that has emerged independently at various positions across the tree of life. It describes the ability of a microorganism to switch to a metabolically inactive state that can withstand unfavorable conditions. However, maintaining such a trait requires additional resources that could otherwise be used to increase e.g. reproductive rates. In this paper, we aim for gaining a basic understanding under which conditions maintaining a seed bank of dormant individuals provides a fitness advantage when facing resource limitations and competition for resources among individuals (in an otherwise stable environment). In particular, we wish to understand when an individual with a dormancy trait can invade a resident population lacking this trait despite having a lower reproduction rate than the residents. To this end, we follow a stochastic individual-based approach employing birth-and-death processes, where dormancy is triggered by competitive pressure for resources. In the large-population limit, we identify a necessary and sufficient condition under which a complete invasion of mutants has a positive probability. Further, we explicitly determine the limiting probability of invasion and the asymptotic time to fixation of mutants in the case of a successful invasion. In the proofs, we observe the three classical phases of invasion dynamics in the guise of Coron et al. (2017, 2019).
We investigate the interplay between two fundamental mechanisms of microbial population dynamics and evolution called dormancy and horizontal gene transfer. The corresponding traits come in many guises and are ubiquitous in microbial communities, affecting their dynamics in important ways. Recently, they have each moved (separately) into the focus of stochastic individual-based modelling (Billiard et al. 2016, 2018; Champagnat, Meleard and Tran, 2021; Blath and Tobias 2020). Here, we examine their combined effects in a unified model. Indeed, we consider the (idealized) scenario of two sub-populations, respectively carrying trait 1 and trait 2, where trait 1 individuals are able to switch (under competitive pressure) into a dormant state, and trait 2 individuals are able to execute horizontal gene transfer, turning trait 1 individuals into trait 2 ones, at a rate depending on the frequency of individuals. In the large-population limit, we examine the fate of a single trait i individual (a mutant) arriving in a trait j resident population living in equilibrium, for $i,j=1,2,i eq j$. We provide a complete analysis of the invasion dynamics in all cases where the resident population is individually fit and the initial behaviour of the mutant population is non-critical. We identify parameter regimes for the invasion and fixation of the new trait, stable coexistence of the two traits, and founder control (where the initial resident always dominates, irrespective of its trait). The most striking result is that stable coexistence occurs in certain scenarios even if trait 2 (which benefits from transfer at the cost of trait 1) would be unfit when being merely on its own. In the case of founder control, the limiting dynamical system has an unstable coexistence equilibrium. In all cases, we observe the classical (up to 3) phases of invasion dynamics `a la Champagnat (2006).
We present models of dormancy in a planktonic culture and in biofilm, and examine the relative advantage of short dormancy versus long dormancy times in each case. Simulations and analyses indicate that in planktonic batch cultures and in chemostats, live biomass is maximized by the fastest possible exit from dormancy. The lower limit of time to reawakening is thus perhaps governed by physiological, biochemical or other constraints within the cells. In biofilm we see that the slower waker has a defensive advantage over the fast waker due to a larger amount of dormant biomass, without an appreciable difference in total live biomass. Thus it would seem that typical laboratory culture conditions can be unrepresentative of the natural state. We discuss the computational methods developed for this work.
In this work, we consider distributed agreement tasks in microbial distributed systems under stochastic population dynamics and competitive interactions. We examine how competitive exclusion can be used to solve distributed agreement tasks in the microbial setting. To this end, we develop a new technique for analyzing the time to reach competitive exclusion in systems with two competing species under biologically realistic population dynamics. We use this technique to analyze a protocol that exploits competitive interactions to solve approximate majority consensus efficiently in microbial systems. To corroborate our analytical results, we use computer simulations to show that these consensus dynamics occur within practical time scales.
In the present article, we investigate the effects of dormancy on an abstract population genetic level. We first provide a short review of seed bank models in population genetics, and the role of dormancy for the interplay of evolutionary forces in general, before we discuss two recent paradigmatic models, referring to spontaneous resp. simultaneous switching of individuals between the active and the dormant state. We show that both mechanisms give rise to non-trivial mathematical objects, namely the (continuous) seed bank diffusion and the seed bank diffusion with jumps, as well as their dual processes, the seed bank coalescent and the seed bank coalescent with simultaneous switching.
This chapter gives a synopsis of recent approaches to model and analyse the evolution of microbial populations under selection. The first part reviews two population genetic models of Lenskis long-term evolution experiment with Escherichia coli, where models aim at explaining the observed curve of the evolution of the mean fitness. The second part describes a model of a host-pathogen system where the population of pathogenes experiences balancing selection, migration, and mutation, as motivated by observations of the genetic diversity of HCMV (the human cytomegalovirus) across hosts.